Well, maybe somebody here can offer something.
I have some notes in regards to the induction and treatment of shock states.
I have tried to follow them out for months now, but have not had any luck.
Here is where I am at.
NfkB,
it is:
proinflammatory
pro thrombotic
but:
antiapoptic
one of the many things that activate it is erythropoietin. Which down regulates IL2 and TNF.
NfkB acting in the nucleus clearly has a greater proinflammatory effect than the erythro. Not suprising since one acts like a steroid and the other like a membrane receptor.
estrogen also has antiapoptotic effects (I cannot figure out if it is from a different receptor than NfkB and can find no research on it.)
Is estrogen synergistic with erythropoietin?
Back to NfkB,
it regulates BCL, which in turn inhibits caspases 3,7,8,9 it also regulates apoptosis by cytochrome C (but I cannot figure out and find no research if it is because it helps cell membrane intergrity of the mitochondria or downregulates cyto C production)
a precursor, AKT, also inhibits bad and bax.
So I am thinking that all of this probably helps to inhibit the onset of apoptosis secondary to cell injury.
But, it doesn't seem to stop the inflammatory response from taking out cells with injured membranes.
It is known that systemic inflammation is a common pathway of shock. There are studies showing antiimmugenic strategies have no effect on outcome.
Does anyone have or know of any studies showing an effect of down regulation of NfkB because I don't have access to any if there are?
Does anyone know anybody who is actively working on this topic I could contact?
I have some notes in regards to the induction and treatment of shock states.
I have tried to follow them out for months now, but have not had any luck.
Here is where I am at.
NfkB,
it is:
proinflammatory
pro thrombotic
but:
antiapoptic
one of the many things that activate it is erythropoietin. Which down regulates IL2 and TNF.
NfkB acting in the nucleus clearly has a greater proinflammatory effect than the erythro. Not suprising since one acts like a steroid and the other like a membrane receptor.
estrogen also has antiapoptotic effects (I cannot figure out if it is from a different receptor than NfkB and can find no research on it.)
Is estrogen synergistic with erythropoietin?
Back to NfkB,
it regulates BCL, which in turn inhibits caspases 3,7,8,9 it also regulates apoptosis by cytochrome C (but I cannot figure out and find no research if it is because it helps cell membrane intergrity of the mitochondria or downregulates cyto C production)
a precursor, AKT, also inhibits bad and bax.
So I am thinking that all of this probably helps to inhibit the onset of apoptosis secondary to cell injury.
But, it doesn't seem to stop the inflammatory response from taking out cells with injured membranes.
It is known that systemic inflammation is a common pathway of shock. There are studies showing antiimmugenic strategies have no effect on outcome.
Does anyone have or know of any studies showing an effect of down regulation of NfkB because I don't have access to any if there are?
Does anyone know anybody who is actively working on this topic I could contact?